Peter U. Tse is a cognitive psychologist and neuroscientist at Dartmouth who argues for a novel form of mental causation that he calls "criterial causation."

The idea is that large numbers of neurons (a complex of cells or "cell assembly") are likely to be involved in even the simplest thoughts and actions. Tse argues that the brain may be able to modify dynamically the probabilities that individual neurons are "firing." He calls this "dynamical synaptic reweighting."

Since the process by which a pre-synaptic neuron releases chemical neurotransmitters into the synaptic cleft is a statistical one (large numbers of neurotransmitter molecules must diffuse across the cleft to activate ion channel receptors on the post-synaptic neuron), Tse says that there is some ontological randomness in the process. He argues that this is real "ontological" indeterministicchance, quantum mechanical in origin.

How exactly such weights or probabilities of firing might work is not understood, but Tse argues that weights would constitute "informational" criteria as opposed to being simply physical. They could represent mental events that supervene on the physical brain events.

Tse accepts the Basic Argument of philosopher Galen Strawson, that we are not free to change the way we are at any moment, that we cannot be "causa sui." But since ontological randomness can dynamically reassign weights to the synapses, we can change mental events in the future. He says:

The central argument against the possibility of free will rests on the impossibility of self-causation. [Strawson's] basic argument does not follow, given a degree of randomness in neural spike timing and given neural criterial causation, as follows: Physically realized mental events can change the physical basis not of themselves in the present, but of future mental events. How? By triggering changes in the physically realized informational/physical criteria for firing that must be met by future neuronal inputs before future neuronal firing occurs that realizes future mental events. Such criterial causation does not involve self-causation.

Tse describes the requirements for a "strong" free will that resembles the requirements for two-stage models of free will, but he does not think of criterial causation as a two-stage model.

In order to have a free will in the strong sense, there must be (a) multiple courses of physical or mental behavior open to us, (b) we must really be able to choose among them, (c) we must be or must have been able to have chosen otherwise once we have chosen, and (d) the choice must not be dictated by randomness alone, but by us.

A strong conception of free will is not compatible with either predetermined or random choices because in neither case do we decide which alternative to actualize from among many that might have been selected.

Criterial causation gets around the causa sui argument against both mental causation and free will by having neurons alter the physical grounds, not of present mental events, but of future mental events.

Self-causation only applies to changing the physical basis of making a present decision that is realized in or supervenes on that very same physical basis. Self-causation does not apply to changing the physical basis of making a future decision. While there can obviously never be a self-caused event, criteria can be set up in advance, such that when they are met, an action automatically follows; this is an action that we will have willed to take place by virtue of having set up those particular criteria in advance. At the moment those criteria are satisfied at some unknown point in the future, leading to some action or choice, those criteria cannot be changed, but because criteria can be changed in advance, we are free to determine how we will behave within certain limits in the near future. Criterial causation therefore offers a path toward free will where a brain can determine how it will behave given particular types of future input. This can be milliseconds in the future or, in some cases, even years away.

Assuming indeterminism, criterial outcome is an outcome that meets certain preset criteria, but what that outcome will be is not foreseeable, and had we run the sequence of events over from the same initial conditions, with the same criteria, we may have ended up with a different outcome, because of noise in the system.

Criterial causality therefore leaves room for non-illusory choice that is a middle path between the extremes of (a) determinism, where there is no ability to choose freely in the strong sense because there is never the possibility of an alternative action, and (b) criteria-less indeterminism, where arbitrary choices follow from randomness rather than from criteria one sets up oneself.

Free will skeptics might counter that the setting up of any set of criteria to be met by future inputs is itself determined by preexisting sets of criteria that have been met. This is in fact correct. The key point is that criteria will be met in unpredictable ways if there is inherent variability or noise in inputs, such as can be introduced by the randomness inherent in neurotransmitter molecules crossing the synapse. Just because new criteria are set up by a nervous system in a manner dictated by the satisfaction of preexisting criteria does not mean that either the future or present criteria will be met in a predetermined manner. Moreover, because our neurons set criteria for the firing of other neurons in response to their future input, the choices realized in the satisfying of those criteria are our own choices. Ontological indeterminism and neuronal criterial causation permits a physical causal basis for a strong free will.

Tse compares his work to traditional two-stage models, but thinks of his criterial causation as having three stages:

The present view is a type of incompatibilist physicalist libertarianism. Its closest relatives are found in Jamesian two-stage models of free will, where a first stage alternative possibilities for action or thought are generated in part randomly, and in a second, subsequent stage, an adequately determined volitional mechanism, where chance is no longer a factor, evaluates and selects the optimal option. James, Popper and others viewed the process as akin to a Darwinian two stage process, where indeterminism in the microscopic domain at the level of genetic reshuffling and mutation is amplified into variability at the level of animal traits, which is then selected among via natural and sexual selection. James and his followers have described the first process as one in which multiple alternative ideas or plans for action are generated in part randomly, and the second stage as one where a will or rational faculty selects from among these possibilities. The present view differs from the traditional Jamesian view in that multiple ideas are not generated, and the selecting faculty is not rational and is not the will, but is instead a postsynaptic neuron. That is, instead of modeling possibility generation and selection at the level of ideas, here the focus is on what happens at the neuronal level. The present view might more profitably be thought of as a three stage model, where (1) in the first stage new physical/informational criteria are set in a neuron or neuronal circuit on the basis of preceding physical/mental processing, including volitional processing, and (2) in the second, later stage inherently variable and therefore indeterministic presynaptic inputs arrive at the post-synaptic neuron, and (3) in the third, later stage physical/informational criteria are met or not met, leading to post-synaptic neural firing or not. Randomness can enter at stage (1)’s resetting of synaptic weights, or in (2)’s presynaptic inputs, but in (3) the threshold for firing is met or not met.

A central argument against the logical possibility of either mental causation or free will has been the impossibility of self-causation: Because mental events, including acts of willing, are realized in or supervene on physical events, they cannot alter the physical events in which they are presently realized or on which they supervene. The central thesis argued here is that physically realized mental events can change the physical basis of future mental events by triggering changes in the physical/informational criteria that must be met by future presynaptic inputs before future neuronal firing occurs. While this process of dynamic resetting of synaptic weights (= resetting of physical/informational criteria for firing) could operate deterministically, if neural processes can amplify were indeterministic, then criteria could be met non-deterministically. Assuming ontological indeterminism, criterial causation permits downward mental causation and free will because neurons can set up criteria for future action potential release which, once satisfied, lead to non-determined, yet self-selected future actions that harness inherent variability in neuronal responses to generate novel solutions that meet the criteria that were set.

Tse believes that neuroscience has been biased by a kind of dogma about neuronal causation that has hampered understanding of mental causation. That traditional view has been that neuronal causation is tantamount to action potentials triggering action potentials. But that is only half the story. The other half is that an action potential can 'rewire' the synaptic weights on a post-synaptic cell without necessarily making it fire. This effectively changes both the connectivity of a neuron in the sense that different inputs might now make it fire than before rapid synaptic resetting, and it potentially changes the informational criteria that must now be met to make the post-synaptic neuron fire.

(Private communication, January 23, 2013)

The Neural Basis of Free Will

In March 2013, MIT Press published Tse's book, The Neural Basis of Free Will: Criterial Causation. In it he argues that criterial causation provides a model for getting around both Galen Strawson's Basic Argument against free will and Jaegwon Kim's logical argument against a non-reductive physicalism and the possibility of mental causation.

Tse defines four "very high demands" of a "strong conception of free will"

I argue that it is possible to be a physicalist and
ontological indeterminist and adhere to a strong conception of free will.
A strong free will requires meeting some very high demands. We must have
(a) multiple courses of physical or mental behavior open to us; (b) we must
really be able to choose among them; (c) we must be or must have been
able to have chosen otherwise once we have chosen a course of behavior;
and (d) the choice must not be dictated by randomness alone, but by us.
This seems like an impossible bill to fill, since it seems to require that acts
of free will involve acts of self-causation. The goal of this chapter is to
describe a way to meet these demands, assuming ontological indeterminism and criterial causation among neurons, that does not fall into the
logical fallacy of self-causation.

(The Neural Basis of Free Will, pp.133-4)

We agree with Tse, and can add some comments and specifics to each of his four demands.

Tse argues that criterial causation allows neurons in the present to alter the physical realization of future mental events in a way that escapes the problem of self causation, namely Galen Strawson's Basic Argument, which Tse thinks has been at the root of basic criticism of the possibility of free will and mental causation.

Let's look closely at Tse's three stages:

(1) in the first stage at t1 new physical/informational criteria are set in a neuron or neuronal circuit on the basis of preceding physical/mental processing, including volitional processing, in part via a mechanism of rapid synaptic resetting that effectively changes
the future inputs to a postsynaptic neuron;

Randomness plays a role here, so resetting the future synaptic weights is not completely "up to us," which was Tse's demand (d) for strong free will.

(2) in the second stage at
later time t2, inherently variable presynaptic inputs arrive at the postsynaptic neuron;

Randomness is also here.

(3) in the third, later stage at t3 physical/informational
criteria are met or not met, leading to postsynaptic neural firing or not.

Note that the conditions in the world (the alternative possibilities) at time t3 may be very different from those at t1, requiring a different response than one that was appropriate at t1. And because the weights set at t1 were random, the "physical realization of future mental events" is not adequately determined. We do not make the choice at t3.

Let's compare Tse's three stages to the traditional two stages of our Cogito model. First the "free" generation of alternative possibilities, involving indeterminism. Second the adequately determined "will" evaluates and selects one of the possibilities. Or we may recursively go back to "think again" before the final decision.

Note that the two-stage model also circumvents Galen Strawson's Basic Argument. It separates the "free" stage of generating possibilities (t1) from the evaluation (t2) and selection "will" stage (t3).

Any criterial outcome will meet the criteria preset by a given
brain and so will be an outcome that is satisfactory to that brain and
caused by that brain, but it will also not be a unique solution predetermined by that brain or coerced upon that brain by external forces. Imagine,
for example, Mozart trying to generate a musical sequence that sounds happy.
Some part of his brain, perhaps a working-memory area like the
dorsal lateral prefrontal cortex, defines criteria that a melody would have
to meet in order to sound happy. Various cascades of criterial satisfaction
are met that result in possible sequences that might meet the happiness
criteria.

These are "presented" to Mozart's executive system, and it either
accepts them or rejects them, whereupon lower level systems continue to
generate possible solutions to the problem. Of course, whatever eventually
is accepted by him as adequate will sound to us like Mozart, because it
satisfied the criterial decoding schemes that were unique to his brain.
However, if we had "rewound the clock," a different solution to the
problem might have been reached than the one that was reached, because
of noise in the system. None of his pieces of music was predestined to
sound as it did, and each piece could have turned out otherwise, although
any piece that met his criteria would have sounded like a piece by Mozart.
He could not help but have his style because he could not help but instantiate criteria that would satisfy Mozart, because he was Mozart, with his nervous
system. Criterial causal systems, like Mozart's brain, can thus
harness randomness to generate novel and creative solutions. His lower-level executive systems generated various sequences that met the criteria
for happiness that his executive decision to generate a happy melody
had set in place.

Note that the second "will" stage can reject the alternative possibilities generated so far, and, time permitting, can ask the first "free" stage to "think again."

When solutions were presented for executive
consideration, his executive system could then further edit these solutions,
or reject them, invoking the further generation of possible solutions
that might meet the criteria set for a happy melody. Indeed, this editing of, selection among, and invoking of solutions to problems appears to be a central function of the executive subsystems of the frontal lobes...

Mozart's executive system was free to reject
or modify possible solutions generated by his lower-level systems that met
his criteria for a musical sequence that sounds happy. This is an open-ended process that can go through countless iterations. Because of noise in the
system, the outcome of this process is not predetermined. It is also
not random. Any outcome will have met Mozart's criteria, so will inevitably end up sounding like Mozart and no one else. Thus, although Mozart was
not free to preset criteria that belonged to Bach, what his nervous
system would create was not foreseeable, in principle, to him or anyone
else. Yet, what he ended up composing was shaped by his nervous system alone
to meet criteria preset by his nervous system.

Criterial causation permits a degree of self-determination that
meets the high standards demanded of a strong free will described in §7.1,
without permitting, of course, a causa sui free will, which is impossible. To reiterate, for us to have a strong free will, multiple courses of physical or
mental behavior must be open to us, we must really be able to choose from
among them, we must have been able to have chosen otherwise once we
have chosen, and the choice must be dictated not by randomness but by us.
Returning to our example, Mozart's brain can generate numerous
musical sequences that meet his preset criteria for a happy melody, and
his executive circuitry can choose from among these on the basis of the
degree to which these criteria are met, or on the basis of other criteria
realized in his nervous system. Because of noise in the system, there is no
guarantee that he would choose the same sequence as the best one if we
could "rewind" him in time and play the sequence over. The same musical
sequences might not even be generated for executive consideration by the
lower-level systems because they in turn generate possible solutions by
setting criteria on their own lower-level inputs, and so on. Such hierarchies
of critical selection can, even at the lowest level, harness noise for the
generation of novel solutions to problems posed by higher levels in the
system. However, the choice is not dictated solely by randomness, but, in the
present example, by criteria that Mozart's nervous system set up to
solve the problem of finding a happy melody. This meets all the stringent
conditions required of a free will described in §7.1, without falling into
the trap of a causa sui free will (§7.4).